pharmacology sheet #9 Adrenal Steroids Mineral corticoids & Glucocorticoids
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1 Adrenal Steroids Mineral corticoids & Glucocorticoids Extra notes : Slide 2: - All Steroids are synthesized in the adrenal gland and secreted from it, It consists of an outer cortex and an inner medulla. Outer cortex: involved in the secretion of Mineralocorticoids (Aldosterone), glucocorticoids (cortisol) middle layer (fasciculata) and androgens and estrogen inner layer( reticularis) in both males and females. Inner medulla :it gives epinephrine and nor epinephrine. Slide 3: Control of synthesis and release of aldosterone: - plasma angiotensin ǁ (the major regulator of aldosterone synthesis and secretion by the adrenal is angiotensin renin system) - potassium blood levels (Aldosterone lowers the potassium blood level and increases sodium blood levels and its more sensitive for potassium levels) -ACTH has a little effect on the aldosterone released by the adrenal, ACTH is mainly involved in controlling cortisol synthesis. Slide 4: Synthesis usually starts from cholesterol by debranching enzyme (desmolase enzyme) into pregnenolone and by dehydrogenase enzyme we get progesterone, where? In the ovaries or breast for example (any place where we need progesterone, It will be formed by the same synthetic machinery from cholesterol) following this a number of hydroxylases will be involved in the synthesis of different steroids (aldosterone, estrogen, androgens, cortisol) so finally we end up with aldosterone,where? In the outer layer of the cortex. We are mentioning this synthetic machinery because we can hit it by drugs and such drugs could be used in the management of excess productions of whatever steroids Slide 5: Renin-angiotensin-aldosterone axis: Angiotensinogen Angiotensin I by Renin which is produced in the kidney Angiotensin I angiotensin II by converting enzyme (ACE) which is produced by the lung mainly, this enzyme converts angiotensin I which has no physiological function,no vasoconstriction vasodilatation effect except for forming angiotensin II which is a very potent vasoconstrictor, it usually increases the synthesis of aldosterone from the adrenal gland. 1 P a g e
2 When we talk about disorders we say primary or secondary hyperaldosteronism, A lot of clinical conditions (ex: heart failure) are involved with secondary hyperaldosteronism. Blood pressure is controlled by a balance between sympathetic, parasympathetic, vasoconstrictors and vasodilators; this axis is one of the substances that is involved in controlling it so any disturbances in the axis could lead to either hypo or hypertension. So hitting this system by drugs would be of a great value in the management of hypertension because these drugs would usually inhibit synthesis of angiotensin II and hence aldosterone Slide 7: Factors/drugs renin-angiotesin-aldosterone: - Angiotensin converting enzyme inhibitors (ACE inhibitors) are highly effective in the management of hypertension, number one drugs to be used in the diuretics patients with hypertension, they are used in combining condition associated with hypertension such as diabetes hypertension number 1 drugs. - Aldosterone antagonists: spironolactone, eplerenone which is more potent and has a longer duration of action. What is the major problem of ACE inhibitors? Dry cough because of the accumulation of bradykinin. As we said before about bradykinin, it's going to be metabolized by kinases and kinase 2 is similar to ACE so what is going to inhibit this enzyme (ACE) is going to inhibit the metabolism of bradykinin and hence It will accumulate leading to dry cough. this is considered an absolute contraindication for it use so If dry cough develops in an individual receiving ACE inhibitor we should stop it, but before that we can change one ACE inhibitor with another (it is not necessarily that if a person develops dry cough to one ACE inhibitor that he will develop the same cough from another ACE inhibitor) but if an individual develops dry cough to more than one ACE inhibitors we should completely stop it, this could lead to death in some cases. - ARB'S (Angiotensin II receptor blockers) and ACE inhibitors: They act the same as they will block aldosterone and the action of angiotensin II and will lead to lowering the blood pressure. So what is the difference between them? We have 2 subtypes for angiotensin II (A and B), A mediates vasoconstriction and B mediates vasodilatation. Angiotensin II receptor blockers will have no effect on bradykinin so they won't develop dry cough (this is the first advantage above ACE inhibitors) even they are known as non cough ACE inhibitors. 2 P a g e
3 The second advantage above ACE inhibitors that angiotensin II receptor blockers usually block selectively angiotensin II A receptor sparing angiotensin II B. ACE inhibitors will inhibit the action of angiotensin II on both receptors. The third advantage is: Angiotensin II is formed by two pathways: the first is this system (Rennin angiotensin aldosterone system) in the blood vessels and the second is by kinases (a group of enzymes that are present in different tissues and will produce angiotensin II ) ACE inhibitors will inhibit angiotensin II that is formed by this axis only, while ARB's will block the action of angiotensin II on angiotensin II A receptors which is formed by both pathways, that s why cardiologists nowadays prefer using ARB's more frequently as compared to ACE Inhibitors, but in fact ACE inhibitors have other advantages not proved in respect to ARB's such as protection from ischemic heart disease even in normal individuals or diabetics. Slide 8: aldosterone effects: - Receptor mediated: we have membrane receptors (very quick action), cytosolic receptors but mainly steroids usually act on nuclear receptors. Slide 9: disorders affecting aldosterone could be primary or secondary - Primary hyperaldosteronism: the initial defect is in the adrenal such as adenomas affecting the cells which secrete aldosterone so it will increase it (hyperaldosteronism), this lead to increase sodium reabsorbtion, expansion of blood volume and lowering effects on renin. - Secondary hyperaldosteronim : is due to hypovolemia (decreased blood volume) this will result in increased renin which enhances aldosterone secretion and release from the adrenal, which will reabsorb water and sodium from the kidney and excretes potassium restoring blood volume. The net effects of aldosterone (most imp. effects) 1. Sodium water retention 2.Hypokalemia so aldosterone is dangerous but its highly controlled and we have many compensatory mechanisms. - Spironolactone (aldosterone antagonists) will produce opposite effects, they are known as potassium sparing diuretics, they lead to excretion of sodium and water and they retain potassium. You should always be careful about potassium blood levels, so whenever you place a patient on a drug that hit or is related to this system you must measure blood potassium levels because hypo or hyperkalemia could lead to fatal cardiac arrhythmia. 3 P a g e
4 Slide 10 : - glucocorticoids are very dangerous and they are considered as magic drugs but they are the last resort treatment except in deficiency state. - cortisol is secreted whenever we need it ( stressful conditions for example ), then negative feedback mechanism will control further synthesis and release. If the problem is deficiency,which could be primary in the adrenal or secondary in the pituitary or tertiary in the hypothalamus,then we should replace it by CRH, ACTH, or cortisol Slide 11 : - Cortisol is secreted in a circadian rhythm, there is variation in the secretion (higher during the day, lower during the night) this will be reversed in individuals who work during the night and sleep during the day that s why you should not change your sleep pattern. - patients who are on glucocorticoid therapy are known as immunocompromised patients - gluucocorticoids are not used only in deficiency state, they are widely used in many clinical situations in individual with normal access (CRH ACTH cortisol), by doing this we are interfering with the endogenous excreting cortisol,because of the negative feedback mechanism,we are suppressing CRH,ACTH and hence cortisol by the adrenals then we are making some sort of atrophy to all these cells. - in many situations glucocorticoids are giving chronically like patients with bronchial asthma known as steroid dependent bronchial asthma (they stay on therapy forever), (if the patient is kept on glucocorticoid therapy no problem) but if you stop glucocorticoid therapy without making sure that you have some source of endogenous secretion of cortisol, minor stress could lead to severe adrenal insufficiency and death! - we have certain tests by which we can assist the function of endogenously secreted cortisol - when we give cortisol therapy in a manner that limits normally secreted cortisol in the body, this will be associated with suppression to the axis so we should give 2/3 of the dose at the morning and 1/3of the dose at the night,and we should not stop it suddenly (gradual withdrawal),, the pituitary needs about 3-6 month to retain back to normal and the adrenal needs almost a year in patients who took cortisol for about 6 months then gradual withdrawal is very essential to them in addition to further tests that assist endogenously secreted cortisol. - Cortisol is synthesized from cholesterol, there is similarity in the two structures with the 4 rings famous nucleus (steroid nucleus). - Observing cortisol structure we can see how many chemical modifications we can make, either by modifying the side chain or the rings in order to have different glucocorticoids with different pharmacological properties (kinetics), not only that, also differences in the affinity of glucocorticoids to the carrier protein(plasma protein) or to the characteristics of the binding of the steroid to the nucleus, if you change such characteristic you end up with glucocorticoid, for example that has low 4 P a g e
5 affinity to the carrier protein but very strong affinity to nuclear receptor, such drugs are going to have short plasma half life but long duration of action (there is no steroid in the plasma but it's still working) - Dexamethasone among the glucocorticoids that is characterized by low affinity to the carrier protein, strong affinity to nuclear receptor, it has no antisteroid like activity and it acts for 1 month. - We can even modify the structure for example: changing the ring to benzene ring by aromatization reaction changes androgen to estrogen. Slide 12-15: - The same synthetic machinery until we end up with cortisol in the middle layer of the cortex. Steroid synthesis inhibitors: - o,p-ddd produces direct toxic effect to the middle and inner layers, very toxic, mainly used in the management of adrenal cancer when surgery or other modalities are not feasible ( unfortunately most of these drugs that hit the synthetic machinery are toxic, but they could be used in the management of excess production of whatever steroid ) - aminoglutethimide : it inhibit desmolase enzyme so it can be used anywhere to inhibit steroid synthesis whether in the adrenal, intestines, ovaries ( it could be used in the management of different states associated with excess production of aldosterone, progesterone, estrogen..) - ketoconazole : antifungal agent,inhibits steroidogenesis in adrenals and testis, relatively save as compared to trilosane and mitotane. - amphenone B : no more used because its very toxic, inhibit different hydroxylases, we mention it because we might reach to synthesizing drugs similar to it but without side effects. - metyrapone (metopirone) : very effective orally,this drug inhibit the last step in cortisol synthesis, and it's usually used to assist the endogenously secreted cotisol while the patient is on exogenous cortisol therapy ( it just inhibit cortisol, not other steroids). We can use it in the management of Cushing's syndrome, the major cause of it is Exogenous cortisol (drug induce), when we give metyrapone to a patient It will inhibit cortisol, then CRH, ACTH will increase a little even If he is on exogenous cortisol, so before we stop giving glucocorticoid therapy, we give metyrapone and measure ACTH before and after, if there is a little increase in ACTH then we safely can stop glucocorticoid. Slide 16: - Glucocorticoid synthesized in the adrenal, secreted into the blood stream, carried by specific globulins reaching target cells, interacting with cytosolic receptors and nuclear receptors, leading to the following side effects and effects : 5 P a g e
6 They break down proteins and decrease their anabolism, this is responsible for most of the side effects of steroids, and it could lead to osteoporosis, skin atrophy, and peptic ulceration Slide 17: - on lipids : Cushing's syndrome is very obvious, truncal obesity with buffalo hump, striae are obvious on the abdomen, this is because cortisol leads to fat redistribution (deposition of fats on some places above other places ) - On electrolytes (very imp.) sodium water retention is a universal side effects to all steroids whether progesterone, estrogen, testosterone, cortisol.., due to aldosterone like effect (similarity in structure ) - aldosterone like effect is considered the major limitation in the development of good glucocorticoid ( in synthesizing glucocorticoid we try as much as possible to have a steroid (cortisol like drug) with good anti-inflammatory and less aldosterone like effect. Major side effect of steroid : suppression to the axis Major limitation in synthesizing a good cortisol: aldosterone like effect Slide : - Potent anti-inflammatory effect (not contraindicated in bronchial asthma, but still contraindicated in patients with peptic ulcer disease because thy inhibit synthesis of protective prostaglandin in the intestine), they act mainly on phospholipase inhibition, inhibiting both pathways cyclooxygenase and lipoxygenase that are involved in inflammation. - Glucocorticoids have also immunosuppressant effect, that s why we say the patient is compromised (the function of the immune system will be decreased), but they don't lead to bone marrow depression unlike other anticancerous agents (advantage) Slide : Glucocortiocids preparation could be oral, IP, even intraarticular, eye drops, etc Some examples of glucocorticoids preparations (Don't memorize numbers) : They took cortisol as a prototype, they assigned a unit to the anti-inflammatory effect and a unit to the aldosterone like activity and they compared the other preparations in respect to these two major effects to cortisol, for example fludrocortisone is 10 times more potent in regards to the anti-inflammatory effect and 150 times regarding aldosterone like activity (we can use it as if it's an aldosterone aldosterone is not used clinically) - Prednisolone is the most widely used preparation, glucocorticoid synthetic analog in all its forms whether oral, parental Slide : clinical uses to glucocorticoids : 6 P a g e
7 - Immunosuppressant effect: organ transplantation, anticancerous effect (they are widely combined with other anticancerous agents in the management of leukemia's, lymphoma's, different breast cancers. Thank you Goodluck Areej Alkilani 7 P a g e
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